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Expression of pro-inflammatory cytokines and the risk of intracranial aneurysm
- Source :
- Inflammation. 36(6)
- Publication Year :
- 2013
-
Abstract
- Intracranial aneurysm (IA) lingers as a potentially devastating clinical problem, in which inflammation acts as a critical contributor to the pathogenesis of this disease. Cytokines play a major role in regulating inflammation. The aim of this study was to gain insight in the inflammatory response in IA by assessing plasma cytokine profiles. Plasma levels of 10 cytokines were quantified by multiplex protein arrays in 66 patients with IA and 78 healthy controls. Results showed that plasma level of interleukin 1 beta (IL-1β) was 2.4-fold higher in patients than in controls (p < 0.05). The level of monocyte chemoattractant protein-1 (MCP-1) was 2.8-fold higher in patient than in controls (p < 0.01). The level of tumor necrosis factor-alpha (TNF-α) was 2.1-fold higher in cases than in controls (p < 0.001). When comparing the expression of cytokines in IA patients with different characteristics, cases with ruptured aneurysm revealed increased level of MCP-1 than those with unruptured aneurysm (p < 0.05), whereas cases with multiple numbers of aneurysms demonstrated higher levels of MCP-1 and TNF-α than those with single aneurysm (p < 0.05 and p < 0.05, respectively). These data indicated that IL-1β, MCP-1, and TNF-α were associated with increased risk of IA and may affect the development of this disease.
- Subjects :
- Male
Risk
Pathology
medicine.medical_specialty
medicine.medical_treatment
Immunology
Interleukin-1beta
Inflammation
Gastroenterology
Proinflammatory cytokine
Pathogenesis
Aneurysm
Internal medicine
Immunology and Allergy
Medicine
Humans
Chemokine CCL2
business.industry
Tumor Necrosis Factor-alpha
Monocyte
Intracranial Aneurysm
Middle Aged
medicine.disease
Rheumatology
Cytokine
medicine.anatomical_structure
Tumor necrosis factor alpha
Female
medicine.symptom
business
Subjects
Details
- ISSN :
- 15732576
- Volume :
- 36
- Issue :
- 6
- Database :
- OpenAIRE
- Journal :
- Inflammation
- Accession number :
- edsair.doi.dedup.....0bd1b85cc89303dc8008b7798537c31d